What is the role of structural abnormalities of the brain in the pathophysiology of precocious puberty?

Updated: Nov 30, 2020
  • Author: Paul B Kaplowitz, MD, PhD; Chief Editor: Robert P Hoffman, MD  more...
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High-amplitude pulses of GnRH from the hypothalamus at the onset of puberty cause pulsatile increases in the pituitary gonadotropins LH and follicle-stimulating hormone (FSH). Increased LH levels stimulate production of sex steroids by testicular Leydig cells or ovarian granulosa cells. Pubertal levels of androgens or estrogens cause the physical changes of puberty, including penile enlargement and sexual hair in boys and breast development in girls. These levels also mediate the pubertal growth spurt. Increased FSH levels cause enlargement of the gonads in both sexes and eventually promote follicular maturation in girls and spermatogenesis in boys. Research has implicated a family of peptides called kisspeptins, produced in the central nervous system (CNS), in the regulation of GnRH secretion.

The hypothesized mechanisms that suppress the onset of puberty in early childhood include (1) the HPG axis, which is highly sensitive to feedback inhibition by small amounts of sex steroids, and (2) central neural pathways that suppress the release of GnRH pulses.

Most patients, particularly girls suspected of having CPP, are otherwise healthy children whose pubertal maturation begins at the early end of the normal distribution curve. CNS imaging studies of these girls aged 6-8 years usually reveal no structural abnormalities. While older studies reported a significant proportion of abnormal findings such as tumors, subsequent reports have found an incidence of clinically significant brain imaging findings of less than 1%, even in girls below age 6 years. [2]  Abnormal computed tomography (CT) or MRI scans are more frequent among boys with CPP than among girls with the condition.

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